Acidosis inhibited arterial increases in glycerol and FFA due to circulating noradrenaline by 60-70%, but did not affect the lipolytic response to locally released noradrenaline from nerve stimulation.
Acidosis inhibits the lipolytic effect of circulating noradrenaline but not locally released noradrenaline from sympathetic nerves in canine adipose tissue.
Abstract The influence of hypercapnic acidosis on the effects of i.v. noradrenaline (NA) infusions and of sympathetic nervous stimulation were studied in the isolated autoperfused subcutaneous adipose tissue of the dog. Acidosis increased resting vascular resistance in the adipose tissue. Infusion of NA (0.35‐0.69, μg/kg/min for 30 min) increased adipose tissue blood flow at both pH 7.4 and 7.0. Arterial increases in glycerol and FFA due to NA infusions were inhibited by 60–70 % during acidosis. Mobilization of these lipolytic products from the adipose tissue was impaired to the same degree. Sympathetic nervous stimulation (4 Hz for 5 min) lead to the same increase in vascular resistance at normal and acid pH. The lipolytic response, i.e. glycerol release, to nerve stimulation was unaffected by acidosis. FFA release was, however, reduced by about 40 %. Release of 3 H‐NA by nerve stimulation from previously labelled adipose tissue was not significantly increased during acidosis. We conclude that inhibition of NA induced increases in arterial glycerol and FFA concentrations by acidosis can be explained by impaired mobilization from the adipose tissue. Furthermore, the lipolytic effect of locally released NA is not inhibited by acidosis, in contrast to the findings with circulating NA. This difference cannot to any major extent be explained by increased transmittor release during acidosis.
Hjemdahl et al. (Sun,) reported a other. Hypercapnic acidosis vs. Normal pH (7.4) was evaluated on Lipolytic activity (glycerol and FFA release). Acidosis inhibited arterial increases in glycerol and FFA due to circulating noradrenaline by 60-70%, but did not affect the lipolytic response to locally released noradrenaline from nerve stimulation.